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Copper deficiency in chicks: effects of ascorbic acid on iron, copper, cytochrome oxidase activity, and aortic mucopolysaccharides

Published online by Cambridge University Press:  09 March 2007

C. E. Hunt
Affiliation:
Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
Joanne Landesman
Affiliation:
Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
P. M. Newberne
Affiliation:
Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
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Abstract

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1. Copper deficiency was induced in newly hatched chicks by feeding on a milk-based diet for 12 d; effects of supplementation with ascorbic acid were studied.

2. Cu deficiency alone resulted in 30% mortality from aortic rupture. This was associated with a 20% increase in total acid mucopolysaccharides in the aorta, manifested as an increase in chondroitin sulphate and a relative decrease in hyaluronic acid. Cytochrome oxidase activity of liver and heart was less than half that of the controls.

3. Supplementing the Cu-deficient diet with 0.5 % L-ascorbic acid increased mortality to 40%, raised total aortic acid mucopolysaccharides to a higher level, and increased liver iron by 36%.

4. Supplementing the control diet with ascorbic acid decreased liver Cu by 30% and significantly reduced total aortic acid mucopolysaccharides.

5. The enhancement of the Cu-deficiency effect by ascorbic acid probably results from interactions between ascorbic acid and absorption or metabolism of Cu; untoward effects of supplementing the control diet with ascorbic acid may be interpreted as manifestations of ascorbic acid toxicity per se.

Type
Research Article
Copyright
Copyright © The Nutrition Society 1970

References

REFERENCES

Armed Forces Institute of Pathology (1960). Manual of Histologic and Special Staining Technics 2nd ed. New York: McGraw–Hill Book Company.Google Scholar
Bush, J. A., Jensen, W. N., Athens, J. W., Ashenbrucker, M., Cartwright, G. E. & Wintrobe, M. M. (1956). J. exp. Med. 103, 701.CrossRefGoogle Scholar
Carlton, W. W. & Henderson, W. (1963).J. Nutr. 81, 200.CrossRefGoogle Scholar
Carlton, W. W. & Henderson, W. (1964 a). Avian Dis. 8, 48.CrossRefGoogle Scholar
Carlton, W. W. & Henderson, W. (1964 b). Avian Dis. 8, 227.CrossRefGoogle Scholar
Carlton, W. W. & Henderson, W. (1965). J. Nutr. 85, 67.CrossRefGoogle Scholar
Chase, M. A., Gubler, C. J., Cartwright, G. E. & Wintrobe, M. M. (1962). J. biol. Chem. 199, 757.CrossRefGoogle Scholar
Coulson, W. F. & Linker, A, (1968). Biochim. biophys. Acta 158, 117.CrossRefGoogle Scholar
Elvehjem, C. A. & Hart, E. B. (1929). J. biol. Chem. 84, 131.CrossRefGoogle Scholar
Gallagher, C. H., Judah, J. D. & Rees, K. R. (1956). Proc. R. Sac. B 145. 134.Google Scholar
Gore, I., Tanaka, Y., Fujinami, T. & Goodman, M. L. (1965). J. Nutr. 87, 311.CrossRefGoogle Scholar
Griffiths, D. E. & Wharton, D. C. (1961). J. biol. Chem. 236, 1850.CrossRefGoogle Scholar
Gubler, C. J., Cartwright, G. E. & Wintrobe, M. M. (1957). J. biol. Chem. 224, 533.CrossRefGoogle Scholar
Hill, C. H. & Matrone, G. (1961). J. Nutr. 73, 425.CrossRefGoogle Scholar
Hill, C. H. & Starcher, B. (1965). J. Nutr. 85, 271.CrossRefGoogle Scholar
Hill, C. H., Starcher, B. & Kim, C. (1967). Fedn Proc. Fedn Am. Socs exp. Biol. 26, 129.Google Scholar
Hopping, J. M. & Ruliffson, W. S. (1966). Am. J. Physiol. 210, 1316.CrossRefGoogle Scholar
Hunt, C. E., Carlton, W. W. & Newberne, P. M. (1970). Br. J. Nutr. 24, 61.CrossRefGoogle Scholar
Kofoed, J. A. & Robertson, W., Van, B. (1966). Biochim. biophys. Acta 124, 86.CrossRefGoogle Scholar
Lemberg, R., Newton, N. & Clarke, L. (1962). Aust. J. exp. Biol. med. Sci. 40, 367.CrossRefGoogle Scholar
Linker, A., Coulson, W. F. & Carnes, W. H. (1964). J. biol. Chem. 239, 1690.CrossRefGoogle Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). J. biol. Chem. 193, 265.CrossRefGoogle Scholar
Morrison, M., Horie, S. & Mason, H. S. (1963). J. biol. Chem. 238, 2220.CrossRefGoogle Scholar
Nacht, S., Lee, G. R., Cartwright, G. E. & Wintrohe, M. M. (1967). Fedn Proc. Fedn Am. Socs exp. Biol. 26, 634.Google Scholar
Neufeld, H. A., Levay, A. N., Lucas, F. V., Martin, A. P. & Stotz, E. (1960). J. biol. Chem. 233, 209.CrossRefGoogle Scholar
O'Dell, B. L., Bird, W. & Ruggles, D. L. (1966). J. Nutr. 88, 9.CrossRefGoogle Scholar
O'Dell, B. L., Hardwick, B. C., Reynolds, G. & Savage, J. E. (1961). Proc. SOC. exp. Biol. Med. 108, 402.CrossRefGoogle Scholar
Partridge, S. M. (1966). Fedn Proc. Fedn Am. Socs exp. Biol. 25, 1023.Google Scholar
Weissman, N., Shields, G. S. & Carnes, W. H. (1963). J. biol. Chem. 238, 3115.CrossRefGoogle Scholar